Bradykinin preconditioning modulates aquaporin-4 expression after spinal cord ischemic injury in rats

• Published in: Brain research Vol. 1246; pp. 11 - 18
• Main Authors: Wei-bing, Xu, Yan-ting, Gu, Yan-feng, Wang, Xu-hua, Lu, Lian-shun, Jia, Gang, Lv
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 30.12.2008; Elsevier
• Subjects: Analysis of Variance; Animals; Aquaporin 4 - metabolism; Aquaporin-4; Biological and medical sciences; Blotting, Western; Bradykinin; Bradykinin - pharmacology; Disease Models, Animal; Gene Expression; Immunohistochemistry; Ischemia - metabolism; Medical sciences; Microscopy, Electron; Neurology; Random Allocation; Rats; Rats, Sprague-Dawley; Spinal Cord - blood supply; Spinal Cord - metabolism; Spinal cord edema; Spinal Cord Injuries - metabolism; Spinal cord ischemia; Vascular diseases and vascular malformations of the nervous system; Spinal cord ischemia; Aquaporin-4; Spinal cord edema; Bradykinin; Edema; Nervous system diseases; Spinal cord; Rat; Rodentia; Central nervous system; Cardiovascular disease; Gene expression; Neuropeptide; Vascular disease; Vertebrata; Mammalia; Animal; Central nervous system disease; Lesion; Spinal cord disease; Preconditioning; Aquaporin
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2008.09.087

Abstract The study investigated whether bradykinin (BK) preconditioning could regulate the expression of aquaporin-4 (AQP4) using an in vivo transient spinal cord ischemia model in rats. BK was infused continuously via the left femoral artery with infusion pump for 15 min (10 µg/kg/min) then we induced ischemia for 20 min and reperfusion for 24 and 72 h respectively. The results demonstrated that the central part of the white matter exhibited loss of perivascular AQP4 and showed a partial recovery toward 72 h of reperfusion. The border zone of white matter was different from the central part of the white matter by showing no loss of perivascular AQP4 at 24 h of reperfusion but rather a slight increase. BK significantly reduced the expression level of AQP4 protein in the white matter, but it had none of this effect in the gray matter region at 72 h post-reperfusion. There was no difference in AQP4 protein levels between BK group and control group at the two above-mentioned spinal cord regions at 24 h after reperfusion. In addition, the changes in AQP4 protein induced by BK preconditioning were obvious at 72 h after reperfusion, which were accompanied by a reduction of spinal cord edema. Our results demonstrated that the expression of AQP4 protein after spinal cord ischemia/reperfusion was region-specific, time-dependent and also indicated that the attenuation of AQP4 expression induced by BK could be one of the important molecular mechanisms in physiopathology of spinal cord ischemic edema.